Publications by authors named "Jinjun Li"

174 Publications

A methodological study on the combination of qualitative and quantitative methods in cognitive interviewing for cross-cultural adaptation.

Nurs Open 2021 Oct 30. Epub 2021 Oct 30.

Department of Nursing, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Aim: The aim of this study is to explore the use of the Questionnaire Appraisal System with a combination of qualitative and quantitative methods in cognitive interviewing for cross-cultural adaptation.

Design: This is a descriptive methodological study.

Methods: Using the Mandarin version of the Post-Stroke Checklist as an example, cognitive interviews were conducted with 27 stroke survivors in Guangzhou between November 2020 and February 2021. The Questionnaire Appraisal System was applied as a codebook in focus group discussions to perform quantitative data collections and quantitative content analysis.

Results: Thirty-eight problems were proposed in focus group discussions and identified all but four of the 30 questions that emerged in the cognitive interviews. A new item was added to the Questionnaire Appraisal System for better categorization. Four categories and six subcategories of problems in the checklist were revealed.
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http://dx.doi.org/10.1002/nop2.1121DOI Listing
October 2021

Microplastics in fish meals: An exposure route for aquaculture animals.

Sci Total Environ 2021 Oct 18:151049. Epub 2021 Oct 18.

Research and Development Center for Efficient Utilization of Coastal Bioresources, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, Yantai 264003, PR China; Center for Ocean Mega-science, Chinese Academy of Sciences, Qingdao, Shandong 266071, PR China; Muping Coastal Environment Research Station, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, Yantai 264003, PR China. Electronic address:

Microplastics (MPs) are widely detected in many marine fishes. Fish meal contaminated by MP may constitute a potential threat to aquaculture animals. This study analyzed the characteristics of MP in fish meals from ten major fish meal-producing countries around the world. Microplastics were isolated from fish meal, examined under a microscope and identified using Fourier transform infrared microspectroscopy (μ-FT-IR). The results showed that MP pollution was widely detected in fish meal samples from ten countries. The average MP abundance of fish meals was 5.5 ± 1.6 items/g, with higher levels in China, Peru and Myanmar, which might be related to the high pollution level in fish and their habitats. In isolated MPs, fibers were the main shape type, and the most common size was 500-1000 μm. A total of 6 polymers were identified, with cellophane (CP), polypropylene (PP) and polyethylene teraphalate (PET) being the most common types. The total amount of MP ingestion from fish meals by different cultured animals was also estimated, with Atlantic salmon Salmon salar ingesting the largest number of MPs (9361 items), and red swamp crayfish Procambarus clarkii ingesting the smallest number of MPs (19 items). Thus, fish meal constitutes an important exposure route of MPs for aquaculture animals. The results of this study will provide a basis to assess the potential health risks of MPs in fish meals around the world.
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http://dx.doi.org/10.1016/j.scitotenv.2021.151049DOI Listing
October 2021

Oxide of porous graphitized carbon as recoverable functional adsorbent that removes toxic metals from water.

J Colloid Interface Sci 2022 Jan 17;606(Pt 2):983-993. Epub 2021 Aug 17.

School of Resource and Environmental Sciences, Wuhan University, Wuhan 430079, China. Electronic address:

The numerous oxygenated functional groups on graphite oxide (GO) make it a promising adsorbent for toxic heavy metals in water. However, the GO prepared from natural graphite is water-soluble after exfoliation, making its recovery for reuse extremely difficult. In this study, porous graphitized carbon (PGC) was oxidized to fabricate a GO-like material, PGCO. The PGCO showed an O/C molar ratio of 0.63, and 8.4% of the surface carbon species were carboxyl, exhibiting enhanced oxidation degree compared to GO. The small PGCO sheets were intensely aggregated chemically, yielding an insoluble solid easily separable from water by sedimentation or filtration. Batch adsorption experiments demonstrated that the PGCO afforded significantly higher removal efficiencies for heavy metals than GO, owing to the former's greater functionalization with oxygenated groups. An isotherm study suggested that the adsorption obeyed the Langmuir model, and the derived maximum adsorption capacities for Cr, Pb, Cu, Cd, Zn, and Ni were 119.6, 377.1, 99.1, 65.2, 53.0, and 58.1 mg/g, respectively. Furthermore, the spent PGCO was successively regenerated by acid treatment. The results of the study indicate that PGCO could be an alternative adsorbent for remediating toxic metal-contaminated waters.
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http://dx.doi.org/10.1016/j.jcis.2021.08.082DOI Listing
January 2022

Correction: Pigment epithelium-derived factor promotes tumor metastasis through an interaction with laminin receptor in hepatocellular carcinomas.

Cell Death Dis 2021 Jul 20;12(8):718. Epub 2021 Jul 20.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200032, China.

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http://dx.doi.org/10.1038/s41419-021-03975-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8292505PMC
July 2021

B-Cell Receptor-Associated Protein 31 Promotes Metastasis AKT/β-Catenin/Snail Pathway in Hepatocellular Carcinoma.

Front Mol Biosci 2021 11;8:656151. Epub 2021 Jun 11.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Hepatocellular carcinoma (HCC) is one of the most lethal cancer worldwide, characterized with high heterogeneity and inclination to metastasize. Emerging evidence suggests that BAP31 gets involved in cancer progression with different kinds. It still remains unknown whether and how BAP31 plays a role in HCC metastasis. Epithelial-mesenchymal transition (EMT) has been a common feature in tumor micro-environment, whose inducer TGF-β increased BAP31 expression in this research. Elevated expression of BAP31 was positively correlated with tumor size, vascular invasion and poor prognosis in human HCC. Ectopic expression of BAP31 promoted cell migration and invasion while BAP31 knockdown markedly attenuated metastatic potential in HCC cells and mice orthotopic xenografts. BAP31 induced EMT process, and enhanced the expression level of EMT-related factor Snail and decreased contents and membrane distribution of E-cadherin. BAP31 also activated AKT/β-catenin pathway, which mediated its promotional effects on HCC metastasis. AKT inhibitor further counteracted the activated AKT/β-catenin/Snail upon BAP31 over-expression. Moreover, silencing Snail in BAP31-overexpressed cells impaired enhanced migratory and invasive abilities of HCC cells. In HCC tissues, BAP31 expression was positively associated with Snail. In conclusion, BAP31 promotes HCC metastasis by activating AKT/β-catenin/Snail pathway. Thus, our study implicates BAP31 as potential prognostic biomarker, and provides valuable information for HCC prognosis and treatment.
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http://dx.doi.org/10.3389/fmolb.2021.656151DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8231437PMC
June 2021

Clinical study of skull repair in the treatment of epilepsy after bone flap decompression in patients with severe brain injury.

Panminerva Med 2021 Jun 11. Epub 2021 Jun 11.

Department of Neurosurgery, Heze Municipal Hospital, Heze, China -

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http://dx.doi.org/10.23736/S0031-0808.21.04425-6DOI Listing
June 2021

Strengthening arsenite oxidation in water using metal-free ultrasonic activation of sulfite.

Chemosphere 2021 Oct 13;281:130860. Epub 2021 May 13.

Faculty of Material Science and Chemistry, China University of Geosciences, Wuhan, 430074, PR China. Electronic address:

Although sulfite-based advanced oxidation processes (AOPs) have received renewed attention due to the production of oxysulfur radicals, the feasibility of using ultrasound (US) to activate sulfite remains unknown. In this work, low frequency ultrasound has been applied for the first time to develop a novel sulfite activation process (US-S(IV)) for enhanced oxidation of arsenite (As(III)). Our results showed that the US-S(IV) process with 1 mM sulfite addition and 20 kHz 650 W ultrasound can achieve approximately 2.9-fold increase in As(III) oxidation rate compared to the US process at pH 7. The mechanisms underpinning the US-S(IV) process have been probed through radical-scavenging experiments and electron spin resonance (ESR) spectrometry. Direct ultrasonolysis of sulfite has been demonstrated to be the predominant pathway producing the primary sulfite radical (SO⁻) in the US-S(IV) process. Besides, the US-S(IV) process also works well in the treatment process of natural water, suggesting that this process could be promising in commercial scale application. This work not only provides a new application of ultrasound in sulfite-based AOP, but also provides further insights into how sulfite impacts the US process.
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http://dx.doi.org/10.1016/j.chemosphere.2021.130860DOI Listing
October 2021

Isomer-Specific Effects of -9,-11- and -10,-12-CLA on Immune Regulation in Ruminal Epithelial Cells.

Animals (Basel) 2021 Apr 19;11(4). Epub 2021 Apr 19.

Institute of Food Sciences, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China.

In this study, we used transcriptomics and qPCR to investigate the potential immunoprotective effects of different conjugated linoleic acid (CLA) isomers, the natural rumen microbial metabolites, on lipopolysaccharide (LPS)-induced inflammation of ruminal epithelial cells (RECs) in vitro. The results showed that 100 μM -10,-12-CLA exerted higher anti-inflammatory effects than -9,-11-CLA by significantly downregulating the expression of genes related to inflammation, cell proliferation and migration in RECs upon LPS stimulation. Transcriptomic analyses further indicated that pretreatment with -10,-12-CLA, but not -9,-11-CLA, significantly suppressed the biological signals of GO terms' response to LPS, the regulation of signal transduction and cytokine production and KEGG pathways NF-κB, chemokine, NOD-like receptor, Hippo, PI3K-Akt, TGF-β and Rap1 signaling in RECs upon LPS stimulation. Furthermore, pretreatment with -10,-12-CLA significantly reduced the expression of lipogenic genes and the biosynthesis of the unsaturated fatty acid pathway in RECs compared with the LPS group, however, -9,-11-CLA exhibited the opposite results. These results suggest the distinct isomer differences of CLA in the regulation of inflammatory responses and adipocytokine signaling in RECs and will provide important references for determining their target use in the future.
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http://dx.doi.org/10.3390/ani11041169DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8072642PMC
April 2021

Upregulation of SKA3 enhances cell proliferation and correlates with poor prognosis in hepatocellular carcinoma.

Oncol Rep 2021 04 24;45(4). Epub 2021 Mar 24.

Department of Hepatic Surgery (Liver Transplantation), The Third People's Hospital of Shenzhen (The Second Affiliated Hospital of Southern University of Science and Technology), Shenzhen, Guangdong 518000, P.R. China.

Hepatocellular carcinoma (HCC) is one of the most aggressive types of malignancy worldwide. However, the mechanism underlying its frequent recurrence remains unclear. Studies have demonstrated that spindle and kinetochore associated complex subunit 3 (SKA3) is highly expressed in colorectal and prostate cancer. The present study aimed to determine whether SKA3 could be a predictive and prognostic marker for liver cancer. SKA3 expression levels in liver cancer cell lines, liver cancer tissues, normal liver cells and non‑cancerous tissues were compared at both transcriptional and translational levels. Correlation between SKA3 levels, clinicopathological characteristics and patient survival was also assessed. Gene set enrichment analysis (GSEA) was performed to identify SKA3‑associated pathways. Furthermore, SKA3 was knocked down and overexpressed in liver cancer cells, and then assessed the effect on cell proliferation, cell cycle, and tumor formation ability. Kaplan‑Meier survival analysis and log‑rank test were used to evaluate the association between SKA3 expression levels and prognosis. SKA3 mRNA and protein expression levels were significantly higher in liver cancer cell lines and clinical samples, compared with normal controls. Immunohistochemical analysis of 110 patients revealed that upregulation of SKA3 correlated with clinical pathological characteristics and patient survival. GSEA showed that BENPORATH_PROLIFERATION gene set signaling pathways were correlated with SKA3 expression levels. Luciferase reporter activity assay revealed that knockdown of SKA3 significantly inhibited the activity of transcription factor E2F. Downregulation of SKA3 significantly inhibited cell proliferation, cell cycle arrest in G‑S phase and tumorigenesis both and , decreased the expression levels of cyclin D1 and phosphorylated‑-retinoblastoma and increased those of p21, suggesting a potential role of SKA3 in mediating tumor cell cycle and progression. SKA3 may function as an oncogene in liver cancer and may be a promising prognostic biomarker and candidate for targeted therapy.
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http://dx.doi.org/10.3892/or.2021.7999DOI Listing
April 2021

Electrochemically driven desaturation of carbonyl compounds.

Nat Chem 2021 04 23;13(4):367-372. Epub 2021 Mar 23.

Department of Chemistry, Scripps Research, La Jolla, CA, USA.

Electrochemical techniques have long been heralded for their innate sustainability as efficient methods to achieve redox reactions. Carbonyl desaturation, as a fundamental organic oxidation, is an oft-employed transformation to unlock adjacent reactivity through the formal removal of two hydrogen atoms. To date, the most reliable methods to achieve this seemingly trivial reaction rely on transition metals (Pd or Cu) or stoichiometric reagents based on I, Br, Se or S. Here we report an operationally simple pathway to access such structures from enol silanes and phosphates using electrons as the primary reagent. This electrochemically driven desaturation exhibits a broad scope across an array of carbonyl derivatives, is easily scalable (1-100 g) and can be predictably implemented into synthetic pathways using experimentally or computationally derived NMR shifts. Systematic comparisons to state-of-the-art techniques reveal that this method can uniquely desaturate a wide array of carbonyl groups. Mechanistic interrogation suggests a radical-based reaction pathway.
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http://dx.doi.org/10.1038/s41557-021-00640-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8049972PMC
April 2021

Calcium Sulfite Solids Activated by Iron for Enhancing As(III) Oxidation in Water.

Molecules 2021 Feb 21;26(4). Epub 2021 Feb 21.

CNRS, SIGMA Clermont, Institut de Chimie de Clermont-Ferrand, Université Clermont Auvergne, F-63000 Clermont-Ferrand, France.

Desulfurized gypsum (DG) as a soil modifier imparts it with bulk solid sulfite. The Fe(III)-sulfite process in the liquid phase has shown great potential for the rapid removal of As(III), but the performance and mechanism of this process using DG as a sulfite source in aqueous solution remains unclear. In this work, employing solid CaSO as a source of SO, we have studied the effects of different conditions (e.g., pH, Fe dosage, sulfite dosage) on As(III) oxidation in the Fe(III)-CaSO system. The results show that 72.1% of As(III) was removed from solution by centrifugal treatment for 60 min at near-neutral pH. Quenching experiments have indicated that oxidation efficiencies of As(III) are due at 67.5% to HO, 17.5% to SO and 15% to SO. This finding may have promising implications in developing a new cost-effective technology for the treatment of arsenic-containing water using DG.
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http://dx.doi.org/10.3390/molecules26041154DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7926685PMC
February 2021

A Positive Feedback Loop of AKR1C3-Mediated Activation of NF-κB and STAT3 Facilitates Proliferation and Metastasis in Hepatocellular Carcinoma.

Cancer Res 2021 03 23;81(5):1361-1374. Epub 2020 Dec 23.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

AKR1C3 is an enzyme belonging to the aldo-ketoreductase family, the members of which catalyze redox transformations involved in biosynthesis, intermediary metabolism, and detoxification. AKR1C3 plays an important role in tumor progression and metastasis, however, little is known about the function and the molecular mechanism underlying the role of AKR1C3 in hepatocellular carcinoma (HCC). In this study, we report that AKR1C3 is significantly upregulated in HCC and that increased AKR1C3 is associated with poor survival. AKR1C3 positively regulated HCC cell proliferation and metastasis and . AKR1C3 promoted tumor proliferation and metastasis by activating NF-κB signaling. Furthermore, AKR1C3 regulated NF-κB activity by modulating TRAF6 and inducing its autoubiquitination in HCC cells. Activation of NF-κB released proinflammatory factors that facilitated the phosphorylation of STAT3 and increased tumor cell proliferation and invasion. Gain- and loss-of-function experiments showed that AKR1C3 promoted tumor proliferation and invasion via the IL6/STAT3 pathway. STAT3 also directly bound the AKR1C3 promoter and increased transcription of AKR1C3, thereby establishing a positive regulatory feedback loop. Treatment with the AKR1C3 inhibitors indocin and medroxyprogesterone acetate inhibited tumor growth and invasion and promoted apoptosis in HCC cells. Collectively, these results indicate that a AKR1C3/NF-κB/STAT3 signaling loop results in HCC cell proliferation and metastasis and could be a promising therapeutic target in HCC. SIGNIFICANCE: These findings elucidate a novel AKR1C3-driven signaling loop that regulates proliferation and metastasis in HCC, providing potential prognostic and therapeutic targets in this disease.
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http://dx.doi.org/10.1158/0008-5472.CAN-20-2480DOI Listing
March 2021

Electroreductive Olefin-Ketone Coupling.

J Am Chem Soc 2020 12 1;142(50):20979-20986. Epub 2020 Dec 1.

Department of Chemistry, Scripps Research, 10550 North Torrey Pines Road, La Jolla 92037, California, United States.

A user-friendly approach is presented to sidestep the venerable Grignard addition to unactivated ketones to access tertiary alcohols by reversing the polarity of the disconnection. In this work a ketone instead acts as a nucleophile when adding to simple unactivated olefins to accomplish the same overall transformation. The scope of this coupling is broad as enabled using an electrochemical approach, and the reaction is scalable, chemoselective, and requires no precaution to exclude air or water. Multiple applications demonstrate the simplifying nature of the reaction on multistep synthesis, and mechanistic studies point to an intuitive mechanism reminiscent of other chemical reductants such as SmI (which cannot accomplish the same reaction).
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http://dx.doi.org/10.1021/jacs.0c11214DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8353665PMC
December 2020

Reciprocal REGγ-mTORC1 regulation promotes glycolytic metabolism in hepatocellular carcinoma.

Oncogene 2021 01 23;40(3):677-692. Epub 2020 Nov 23.

Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, 500 Dongchuan Road, Shanghai, 200241, China.

Despite significant progression in the study of hepatocellular carcinoma (HCC), the role of the proteasome in regulating cross talk between mTOR signaling and glycolysis in liver cancer progression is not fully understood. Here, we demonstrate that deficiency of REGγ, a proteasome activator, in mice significantly attenuates DEN-induced liver tumor formation. Ablation of REGγ increases the stability of PP2Ac (protein phosphatase 2 catalytic subunit) in vitro and in vivo, which dephosphorylates PRAS40 (AKT1 substrate 1) and stabilizes the interaction between PRAS40 and Raptor to inactive mTORC1-mediated hyper-glycolytic metabolism. In the DEN-induced animal model and clinical hepato-carcinoma samples, high levels of REGγ in HCC tumor regions contribute to reduced expression of PP2Ac, leading to accumulation of phosphorylated PRAS40 and mTORC1-mediated activation of HIF1α. Interestingly, mTORC1 enhances REGγ activity in HCC, forming a positive feedback regulatory loop. In conclusion, our study identifies REGγ-PP2Ac-PRAS40 axis as a new layer in regulating mTORC1 activity and downstream glycolytic alterations during HCC development, highlighting the REGγ-proteasome as a potential target for personalized HCC therapy.
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http://dx.doi.org/10.1038/s41388-020-01558-8DOI Listing
January 2021

Lymph Node Ratio-Based Staging System for Gallbladder Cancer With Fewer Than Six Lymph Nodes Examined.

Front Oncol 2020 25;10:542005. Epub 2020 Sep 25.

Department of Pathology, Soochow University Medical School, Suzhou, China.

Purpose: The 8th edition of the American Joint Committee on Cancer (AJCC) tumor-lymph node-metastasis (TNM) staging system for gallbladder cancer (GBC) recommended that at least six lymph nodes (LNs) should be examined. But most patients with GBC had fewer than six LNs resected. This study aimed to establish an alternative index for assessing the LN status during the staging system for GBC patients with fewer than six LNs retrieved.

Patients And Methods: Patient data was extracted from the Surveillance, Epidemiology, and End Results (SEER) database (cases between 2004 and 2013). X-tile software was used to determine the optimal cutoff value for lymph node ratio (LNR) and a concordance index (C-index) was used to evaluate the discriminatory powers of the two staging systems.

Results: The majority of GBC patients in our cohort (1353, 78.5%) had fewer than six LNs examined. Among patients with inadequate LN examination, the higher number of LNs examined correlated with a lower proportion of patients. Using the TNM staging system, the C-index for patients with fewer than six LNs and patients with six or more LNs screened were 0.636 and 0.704, respectively. Using the staging system based on LNR (TNrM), the C-index for patients with fewer than six LNs retrieved and patients with six or more LNs retrieved were 0.649 and 0.694, respectively. Similar results were observed in patients with gallbladder adenocarcinoma (GBA).

Conclusion: TNrM might be superior to the 8th AJCC TNM staging system for stratifying GBC patients with fewer than six LNs examined, and it can complement TNM for more accurate risk stratification. Future prospective studies are needed to validate our findings.
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http://dx.doi.org/10.3389/fonc.2020.542005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7546035PMC
September 2020

Correction: Upregulation of SNX5 predicts poor prognosis and promotes hepatocellular carcinoma progression by modulating the EGFR-ERK1/2 signaling pathway.

Oncogene 2020 Oct;39(41):6511

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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http://dx.doi.org/10.1038/s41388-020-01440-7DOI Listing
October 2020

Cyclodextrin-mediated formation of porous RNA nanospheres and their application in synergistic targeted therapeutics of hepatocellular carcinoma.

Biomaterials 2020 12 7;261:120304. Epub 2020 Aug 7.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200032, PR China. Electronic address:

Spherical and porous nanoparticles are ideal nanostructures for drug delivery. But currently they are mainly composed of non-degradable inorganic materials, which hinder clinical applications. Here, biological porous nanospheres using RNA as the building blocks and cyclodextrin as the adhesive were synthesized. The RNA contained the aptamer of EpCAM for targeting delivery and siRNA for gene silencing of EpCAM, while cyclodextrin could load insoluble sorafenib, the core drug of targeted therapy for hepatocellular carcinoma (HCC), through its hydrophobic cavity. After being internalized into targeted HCC cells under the assistance of the aptamer, the porous nanospheres could be degraded by the cytoplasmic Dicer enzymes, releasing siRNA and sorafenib for synergistic therapy. The synergistic efficacy of the porous RNA nanospheres has been validated at in vitro function assay, subcutaneous tumor bearing mice, and orthotopic tumor bearing mice in vivo models. In view of the broad prospects of synergy of gene therapy with chemotherapy, and the fact that RNA and cyclodextrin of the porous nanospheres can be extended to load various types of siRNA and small molecule drugs, respectively, this form of biological porous nanospheres offers opportunities for targeted delivery of suitable drugs for treatment of specific tumors.
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http://dx.doi.org/10.1016/j.biomaterials.2020.120304DOI Listing
December 2020

Metal-Free Electro-Activated Sulfite Process for As(III) Oxidation in Water Using Graphite Electrodes.

Environ Sci Technol 2020 08 10;54(16):10261-10269. Epub 2020 Aug 10.

Faculty of Material Science and Chemistry, China University of Geosciences, Wuhan 430074, P. R. China.

Transition-metal-activated sulfite [S(IV)] processes for water decontamination have recently received intense attention in the field of decontamination by advanced oxidation processes (AOPs). However, the drawback with respect to the secondary metal sludge contamination involved in various AOPs has been argued often. In this work, we developed a novel electro-sulfite (ES) process using stable and low-cost graphite electrodes to address that concern. Arsenite [As(III)] was used as the target compound for removal by the ES process because of its wide presence and high toxicity. Parameters, including cell voltage, S(IV) concentration, solution pH, and water matrix, and the mechanisms for reactions on anode and cathode were investigated in electrolytic cells containing one or two compartments, respectively. The results show that the ES process using 1 mM S(IV) and 2 V cell voltage oxidizes 5 μM As(III) at a rate of 0.127 min, which is 15-fold higher than mere electrolysis without S(IV) addition (0.008 min) at pH 7. Further studies using radical scavengers and electron spin resonance assays demonstrated that oxysulfur radicals (, SO and SO) and HO are responsible for As(III) oxidation in the ES process. However, HO produced the oxygen reduction reaction in the EO process plays a major role in As(III) oxidation, which explains the lower reaction rate in the absence of S(IV). The effectiveness of the ES process was moreover evidenced by 60-82% As(III) oxidation in field water within 40 min. Overall, this work realizes the metal-free activation of S(IV) and significantly leverages the S(IV)-based water treatment technologies.
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http://dx.doi.org/10.1021/acs.est.9b07078DOI Listing
August 2020

Analysis of Lumbar Sagittal Curvature in Spinal Decompression and Fusion for Lumbar Spinal Stenosis Patients under Roussouly Classification.

Biomed Res Int 2020 1;2020:8078641. Epub 2020 May 1.

Department of Orthopedics, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.

To evaluate the clinical significance of spinal decompression and fusion for lumbar spinal stenosis in old patients under Roussouly classification, 160 old patients (>60 year old) with lumbar spinal stenosis underwent spinal decompression, and fusion were retrospectively studied. According to Roussouly classification, patients were divided into 4 groups, in which Roussouly types I, II, and IV were the nonstandard group and Roussouly type III was the standard group. Visual analog scale (waist, leg) and Oswestry disability index (ODI) scores were recorded before operation and at the final follow-up. All patients improved the sagittal curvature: for patients in Roussouly types I and II, there were statistically significant differences in terms of postoperative global lordosis (GL), global kyphosis (GK), sacral slope (SS), sagittal vertical axis (SVA), and pelvic tilt (PT) compared with that before surgery (all < 0.001); patients in Roussouly type IV obtained similar results with type III after surgery. The four groups showed significant improvement in ODI and VAS scores at final follow-up (all < 0.001). After regrouping at the final follow-up, the proportion of the standard type (Roussouly type III) patients was increased compared with preoperative. In conclusion, Roussouly classification has important guiding significance in spinal decompression and fusion for old patients (>60 years) with lumbar spinal stenosis.
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http://dx.doi.org/10.1155/2020/8078641DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7222496PMC
March 2021

ZNF143-Mediated H3K9 Trimethylation Upregulates CDC6 by Activating MDIG in Hepatocellular Carcinoma.

Cancer Res 2020 06 20;80(12):2599-2611. Epub 2020 Apr 20.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Zinc finger protein 143 (ZNF143) belongs to the zinc finger protein family and possesses transcription factor activity by binding sequence-specific DNA. The exact biological role of ZNF143 in hepatocellular carcinoma (HCC) has not been investigated. Here we report that ZNF143 is overexpressed in HCC tissues and its overexpression correlates with poor prognosis. Gain- and loss-of-function experiments showed that ZNF143 promoted HCC cell proliferation, colony formation, and tumor growth and . ZNF143 accelerated HCC cell-cycle progression by activating cell division cycle 6 (CDC6). Mechanistically, ZNF143 promoted expression of CDC6 by directly activating transcription of histone demethylase mineral dust-induced gene (MDIG), which in turn reduced H3K9me3 enrichment in the CDC6 promoter region. Consistently, ZNF143 expression correlated significantly with MDIG and CDC6 expression in HCC. Collectively, we propose a model for a ZNF143-MDIG-CDC6 oncoprotein axis that provides novel insight into ZNF143, which may serve as a therapeutic target in HCC. SIGNIFICANCE: These findings describe the mechanism by which ZNF143 promotes HCC proliferation and provide important clues for exploring new targets and strategies for clinical treatment of human liver cancer.
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http://dx.doi.org/10.1158/0008-5472.CAN-19-3226DOI Listing
June 2020

Upregulation of SNX5 predicts poor prognosis and promotes hepatocellular carcinoma progression by modulating the EGFR-ERK1/2 signaling pathway.

Oncogene 2020 03 9;39(10):2140-2155. Epub 2019 Dec 9.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Endocytosis is an essential component of cell motility, which facilitates the malignant behavior of cancer. Sorting nexin (SNX) family members are associated with tumor progression. However, the role and mechanism of SNX5 in hepatocellular carcinoma (HCC) progression remain largely unknown. In this study, we investigated the clinical significance and possible involvement of SNX5 in the progression of HCC. Here, we showed that SNX5 was upregulated in tumors compared with adjacent nontumorous tissues in HCC patients. The upregulation of SNX5 in HCC was associated with vascular invasion, intrahepatic metastasis, and poor prognosis. The overexpression of SNX5 promoted HCC cell proliferation, migration, invasion, and metastasis, whereas silencing SNX5 expression resulted in decreased cell proliferation, migration, and invasion. Knockdown of SNX5 significantly inhibited HCC cell proliferation by inducing G1/S transition arrest. Mechanistically, we demonstrated that SNX5 promoted cell proliferation, migration, and invasion via the activation of the EGFR-ERK1/2 pathway by blocking EGF-mediated EGFR internalization. We found that SNX5 interacted with EGFR in HCC cells. Moreover, SNX5-induced cell proliferation, migration, and invasion were partially reversed by the knockdown of EGFR or by ERK1/2 inhibitors. In addition, we demonstrated that SNX5 knockdown sensitized HCC cells to tyrosine kinase inhibitors, including erlotinib and sorafenib. Taken together, our results indicate that SNX5 promotes HCC cell proliferation and metastasis via inhibiting the endocytosis and degradation of EGFR, thereby activating the ERK1/2 signaling pathway. Our work also suggests that SNX5 is a potential therapeutic target for HCC.
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http://dx.doi.org/10.1038/s41388-019-1131-9DOI Listing
March 2020

Optimizing a production strategy for a nonspecific nuclease from Yersinia enterocolitica subsp. palearctica in genetically engineered Escherichia coli.

FEMS Microbiol Lett 2019 12;366(24)

Antibiotics Research and Re-evaluation Key Laboratory of Sichuan Province, Sichuan Industrial Institute of Antibiotics, Chengdu University, Chengdu, China.

A nuclease from Yersinia enterocolitica subsp. palearctica (Nucyep) is a newly found thermostable nonspecific nuclease. The heat-resisting ability of this nuclease would be extremely useful in biological research or pharmaceutical production. However, the application of this nuclease is limited because of its poor yield. This research aimed to improve Nucyep productivity by producing a novel genetically engineered Escherichia coli and optimizing the production procedures. After 4 h of induction by lactose, the new genetically engineered E. coli can express a substantial amount of Nucyep in the form of inclusion bodies. The yield was approximately 0.3 g of inclusion bodies in 1 g of bacterial pellets. The inclusion bodies were extracted by sonication and solubilized in an 8 M urea buffer. Protein renaturation was successfully achieved by dilution method. Pure enzyme was obtained after subjecting the protein solution to anion exchange. The Nucyep showed its nonspecific and heat resistant properties as previously reported (Boissinot et  al. 2016). Through a quantification method, its activity was determined to be 1.3 × 10 6 Kunitz units (K.U.)/mg. These results can serve as a reference for increasing Nucyep production.
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http://dx.doi.org/10.1093/femsle/fnz208DOI Listing
December 2019

TCF12 promotes the tumorigenesis and metastasis of hepatocellular carcinoma via upregulation of CXCR4 expression.

Theranostics 2019 12;9(20):5810-5827. Epub 2019 Aug 12.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200032, China.

TCF12, which is known to be involved in the regulation of cell growth and differentiation, has been reported to function as an oncogene or a tumor suppressor gene in the progression of various malignant tumors. However, its function and molecular mechanism in hepatocellular carcinoma (HCC) remain unclear. Stable ectopic TCF12 expression or knockdown in HCC cell lines was established by lentiviral infection. Then, MTT, colony formation, migration, invasion and HUVECs tube formation assays as well as an orthotopic xenograft model were used to investigate the biologic function of TCF12 in HCC cells and . Subsequently, RNA-Seq analysis was utilized to explore the target genes regulated by TCF12. RT-qPCR, western blotting, a dual-luciferase reporter assay, Ch-IP, CHIP-Seq and functional rescue experiments were used to confirm the target gene regulated by TCF12. Finally, RT-qPCR, western blot and immunohistochemical (IHC) staining were performed to detect the expression level of TCF12 and to analyze the correlation of TCF12 with downstream genes as well as the clinical significance of TCF12 in human primary HCC. Our functional studies revealed that stable overexpression of TCF12 in human HCC cells enhanced cell proliferation, migration and invasion and , whereas knockdown of TCF12 showed opposing effects. Mechanistically, CXCR4 was a downstream target of TCF12, and TCF12 directly bound to the CXCR4 promoter to regulate its expression. Moreover, CXCR4, with its ligand CXCL12, played a critical role in tumor progression induced by TCF12 via activation of the MAPK/ERK and PI3K/AKT signaling pathways. Clinically, IHC analysis revealed that TCF12 was significantly associated with poor survival of HCC patients and that TCF12 expression was closely correlated with CXCR4 expression in primary HCC tissues. Our findings are the first to indicate that TCF12 could promote the tumorigenesis and progression of HCC mainly by upregulating CXCR4 expression and is a prognostic indicator for patients with HCC.
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http://dx.doi.org/10.7150/thno.34973DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6735379PMC
August 2020

HIF-1α-induced RIT1 promotes liver cancer growth and metastasis and its deficiency increases sensitivity to sorafenib.

Cancer Lett 2019 Sep 24;460:96-107. Epub 2019 Jun 24.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200032, China. Electronic address:

Ras-like-without-CAAX-1 (RIT1) belongs to the RAS superfamily of small GTPases, which plays critical roles in tumor progression. However, little is known about the roles of RIT1 in hepatocellular carcinoma (HCC). Here we found that RIT1 expression was positively associated with the presence of intrahepatic metastasis and the histological grade of HCC and higher RIT1 expression indicated shorter overall survival in HCC patients. In vitro and in vivo studies revealed that RIT1 functioned as an oncogene, as overexpression of RIT1 enhanced HCC cell proliferation and aggressive behavior, whereas silencing RIT1 expression repressed the malignant behaviors. Furthermore, RIT1 deficiency increased drug sensitivity to sorafenib treatment. We further demonstrated that hypoxia-inducible factor 1α (HIF-1α) directly transcriptionally upregulated RIT1, and its stableness was positively correlated with RIT1 expression in HCC tissues. Knockdown of RIT1 attenuated the invasion and migration induced by hypoxia. Collectively, our data highlight the significance of HIF-1α/RIT1 axis in driving HCC progression and sorafenib resistance.
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http://dx.doi.org/10.1016/j.canlet.2019.06.016DOI Listing
September 2019

Exploring the Extended Biological Functions of the Human Copper Chaperone of Superoxide Dismutase 1.

Protein J 2019 08;38(4):463-471

Antibiotics Research and Re-evaluation Key Laboratory of Sichuan Province, Sichuan Industrial Institute of Antibiotics, Chengdu University, No. 168 Huaguan Road, Chenghua District, Chengdu, 610052, China.

The human copper chaperone of SOD1 (designated as CCS) was discovered more than two decades ago. It is an important copper binding protein and a homolog of Saccharomyces cerevisiae LYS7. To date, no studies have systematically or specifically elaborated on the functional development of CCS. This review summarizes the essential information about CCS, such as its localization, 3D structure, and copper binding ability. An emphasis is placed on its interacting protein partners and its biological functions in vivo and in vitro. Three-dimensional structural analysis revealed that CCS is composed of three domains. Its primary molecular function is the delivery of copper to SOD1 and activation of SOD1. It has also been reported to bind to XIAP, Mia40, and X11α, and other proteins. Through these protein partners, CCS is implicated in several vital biological processes in vivo, such as copper homeostasis, apoptosis, angiogenesis and oxidative stress. This review is anticipated to assist scientists in systematically understanding the latest research developments of CCS for facilitating the development of new therapeutics targeting CCS in the future.
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http://dx.doi.org/10.1007/s10930-019-09824-9DOI Listing
August 2019

CD24 isoform a promotes cell proliferation, migration and invasion and is downregulated by EGR1 in hepatocellular carcinoma.

Onco Targets Ther 2019 28;12:1705-1716. Epub 2019 Feb 28.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China,

Introduction: CD24 is known as a heavily glycosylated cell surface molecule that is highly expressed in a wide variety of human malignancies. Previous studies have shown that CD24 plays an important role in self-renewal, proliferation, migration, invasion and drug resistance of hepatocellular carcinoma (HCC). However, little is known about the expression and function of CD24 isoform a (CD24A) and CD24 isoform b (CD24B) in HCC.

Materials And Methods: Quantitative real-time polymerase chain reaction (qPCR) and Western blotting were performed to detect CD24 and EGR1 expression in HCC cells and tissue. The function of CD24 in cell proliferation was verified with MTT assays, colony formation assays and tumor xenograft models. Wound healing assays and invasion assays were performed to clarify the function of CD24 in the regulation of cell migration and invasion in HCC. A dual luciferase reporter assay and chromatin immunoprecipitation assay were used to analyze the regulation mechanism of CD24A.

Results: CD24A but not CD24B, which was barely detected by qPCR and Western blotting, is significantly upregulated in HCC tissue. Both CD24A and CD24B contribute to HCC cell proliferation, migration and invasion, but CD24A is more effective than CD24B. EGR1 downregulates CD24A and exerts transcription-promoting activity on the promoter. Furthermore, EGR1 represses HCC cell proliferation via downregulation of CD24A.

Conclusion: CD24A is the predominant CD24 isoform in HCC and plays a major role in cell proliferation, migration, and invasion. EGR1 can exert its antitumor effect through transcriptional downregulation of CD24A in HCC.
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http://dx.doi.org/10.2147/OTT.S196506DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400134PMC
February 2019

Rpn10 promotes tumor progression by regulating hypoxia-inducible factor 1 alpha through the PTEN/Akt signaling pathway in hepatocellular carcinoma.

Cancer Lett 2019 04 20;447:1-11. Epub 2019 Jan 20.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. Electronic address:

The ubiquitin-proteasome pathway plays a pivotal role in tumor progression. Rpn10 is the major ubiquitin (Ub) receptor of the 26S proteasome. Mounting evidence shows that Rpn10 is associated with the progression of several tumor types. However, little is known regarding the mechanistic role of Rpn10 in hepatocellular carcinoma (HCC). In this study, we found that the upregulation of Rpn10 in HCC was associated with poor prognosis. The ectopic overexpression of Rpn10 increased HCC cell proliferation, whereas silencing Rpn10 expression resulted in decreased cell proliferation. Furthermore, we demonstrated that knockdown of Rpn10 induced cell cycle arrest at G1 phase in HCC cells. In addition, we found that Rpn10 increased cell proliferation via regulation of the PTEN/Akt pathways. Knockdown of Rpn10 induced suppression of cell proliferation could be reversed by overexpressing active Akt in HCC cells. Rpn10 directly promoted PTEN degradation through the ubiquitin-proteasome system. The transcription factor HIF1α directly bound to the Rpn10 promoter and increased its expression in HCC tissue. Moreover, we observed a significant correlation between HIF1α expression and Rpn10 levels in HCC patients and found that the combination of these two parameters was a more powerful predictor of poor prognosis than either parameter alone. Collectively, these findings highlight the molecular mechanism of Rpn10 expression in HCC and provide valuable information for cancer prognosis and treatment.
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http://dx.doi.org/10.1016/j.canlet.2019.01.020DOI Listing
April 2019

Inhibitor of binding/differentiation 2 (Id2) is regulated by CCAAT/enhancer-binding protein-α (C/EBPα) and promotes the proliferation of hepatocellular carcinoma.

Am J Cancer Res 2018 1;8(11):2254-2266. Epub 2018 Nov 1.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200032, PR China.

Inhibitor of DNA binding/differentiation (Id2) is an important regulator involved in the initiation and progression of cancer. However, the function and mechanism of the regulation of Id2 in hepatocellular carcinoma (HCC) was unclear. In the present study, we found that the overexpression of Id2 increased HCC cell proliferation and . Knockdown of Id2 inhibited HCC cell proliferation and . Furthermore, knockdown of Id2 enhanced sorafenib-induced apoptosis in HCC. Conversely, overexpression of Id2 weakened sorafenib-induced apoptosis in HCC. In addition, the transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) bound to the Id2 promoter and decreased its expression in HCC cells. Therefore, all results suggest that Id2 promotes the proliferation of HCC cells by inhibiting cell apoptosis. Id2 may serve as a potential target in HCC therapy.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6291656PMC
November 2018

ATF3 inhibits the tumorigenesis and progression of hepatocellular carcinoma cells via upregulation of CYR61 expression.

J Exp Clin Cancer Res 2018 Oct 30;37(1):263. Epub 2018 Oct 30.

State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, 25/Ln 2200 Xietu Road, Shanghai, 200032, China.

Background: Hepatocellular carcinoma (HCC) is one of the most common malignant cancers with a high incidence and high mortality in East Asia. Identifying biomarkers and clarifying the regulatory mechanisms of HCC are of great importance. Herein, we report the role and mechanism of activating transcription factor 3 (ATF3), a member of the ATF/cAMP-responsive element-binding protein family of transcription factors in HCC.

Methods: ATF3 overexpression vector and shRNAs were transfected into HCC cancer cells to upregulate or downregulate ATF3 expression. In vitro and in vivo assays were performed to investigate the functional role of ATF3 in hepatocellular carcinoma. RNA-Seq was performed to screen the differentially expressed genes downstream of ATF3. The dual-luciferase reporter assay, chromatin immunoprecipitation (Ch-IP) analysis and functional rescue experiments were used to confirm the target gene regulated by ATF3. Tissue microarrays (TMAs) comprising 236 human primary HCC tissues were obtained and immunohistochemical staining were carried out to analyze the clinical significance of ATF3.

Results: The results indicate that ATF3 significantly inhibited the proliferation and mobility of HCC cells both in vitro and in vivo. Cysteine-rich angiogenic inducer 61 (CYR61) is a key target for transcriptional regulation by ATF3. Both ATF3 and CYR61 were consistently downregulated in human HCC tissues, and their expression levels were significantly and positively correlated with each other.

Conclusions: Our findings indicate that ATF3 functions as a tumor suppressor in HCC through targeting and regulating CYR61.
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http://dx.doi.org/10.1186/s13046-018-0919-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6208028PMC
October 2018

Enzymatic synthesis of cefazolin using immobilized recombinant cephalosporin-acid synthetase as the biocatalyst.

Bioprocess Biosyst Eng 2018 Dec 22;41(12):1851-1867. Epub 2018 Sep 22.

State Research Institute for Genetics and Selection of Industrial Microorganisms of National Research Center "Kurchatov Institute" (NRC "Kurchatov Institute"-GOSNIIGENETIKA), 1st Dorozhny proezd, 1, Moscow, 117545, Russia.

A method for the synthesis of β-lactam antibiotic cefazolin (CEZ) by enzymatic acylation of 7-amino-3-(5-methyl-l,3,4-thiadiazol-2-yl)thiomethyl-3-cephem-4-carboxylic acid (TDA) using immobilized cephalosporin-acid synthetase (IECASA) from recombinant E. coli strain VKPM B-12316 has been developed. A stepwise pH gradient designed on the basis of investigations on the solubility of components was applied for synthesis. This helped in avoiding the precipitation of TDA in the reaction when its initial concentration was high (150-200 mM). Thus, under optimal conditions a high yield of CEZ (relative to TDA) of 92-95% was obtained. Where the final reaction mixture contained 65-85 mg/mL of CEZ, 4-5 mg/mL of unreacted TDA, and 40-60 mg/mL of the by-product, 1(H)-tetrazolylacetic acid (TzAA). Testing of optimized CEZ synthesis using IECASA in a batch reactor has proved sufficiently high operational stability of the biocatalyst, with its residual activity after the 25th cycle accounting for about 83 ± 2% of its starting value. The half-inactivation period of IECASA was estimated as 85 cycles of CEZ synthesis.
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http://dx.doi.org/10.1007/s00449-018-2007-zDOI Listing
December 2018
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